Propionibacterium acnes induces cartilaginous endplate degeneration by promoting MIF expression via the NF-κB pathway

• Main Authors: Ying Zhang, Yuting Wang, Yanyan Yuan, Yeting Lin, Binbin Lin, Haiyan Zhou
• Format: Article
• Language: English
• Published: BMC 2020-06-01
• Series: Journal of Orthopaedic Surgery and Research
• Subjects: Cartilaginous endplate degeneration; Macrophage migration inhibitory factor; Propionibacterium acnes; NF-κB pathway; Inflammatory cytokines
• Online Access: http://link.springer.com/article/10.1186/s13018-020-01714-6
• ISSN: 1749-799X

Abstract Background Propionibacterium acnes (P. acnes) is a novel pathogenic factor that contributes to cartilaginous endplate (CEP) degeneration. However, the underlying mechanism of P. acnes-induced CEP degeneration remains unclear. The objective of this study is to investigate the underlying mechanism of P. acnes-induced CEP degeneration. Methods We first examined MIF expression in degenerated human CEP samples by immunohistochemistry. We developed a P. acnes-induced rat model and detected MIF expression using immunohistochemistry. Additionally, we investigated the mechanism of P. acnes-induced CEP degeneration in CEP cells using western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results We found that compared with the normal human CEP, the expression of MIF was increased in the degenerated human CEP. In a rat model, P. acnes induced CEP degeneration and upregulated MIF expression significantly. More importantly, we revealed the underlying mechanism of P. acnes-induced CEP degeneration in the rat CEP cells. Firstly, P. acnes induced the expression of MIF in a concentration-dependent manner. Then, MIF upregulated the expression of MMP-13 and promoted the secretion of IL-6 and IL-1β. Finally, P. acnes may promote MIF expression via NF-κB pathway rather than ERK1/2 pathway. Conclusion P. acnes-induced MIF expression via NF-κB pathway may be the underlying mechanism of CEP degeneration.